T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice

Li, Bobby W. S.; Bruijn, Marjolein J. W. de; Lukkes, Melanie; Nimwegen, Menno van; Bergen, Ingrid M.; KleinJan, Alex; GeurtsvanKessel, Corine H.; Andeweg, Arno C.; Rimmelzwaan, Guus F.

doi:10.1002/eji.201747421

Cited by 42 publications

(50 citation statements)

References 64 publications

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“…During influenza infection, ILC2s can also be activated, although at a late stage. 117 However, whether some of these ILC2s will display a partial ILC1-like phenotype and whether conversion of some ILC2s to ILC1s has occurred in this infection setting is unknown.…”

Section: Type 2 Immune Response Mediated By Ilc2smentioning

confidence: 99%

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

2019

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The type 2 immune response is critical for host defense against large parasites such as helminths. On the other hand, dysregulation of the type 2 immune response may cause immunopathological conditions, including asthma, atopic dermatitis, rhinitis, and anaphylaxis. Thus, a balanced type 2 immune response must be achieved to mount effective protection against invading pathogens while avoiding immunopathology. The classical model of type 2 immunity mainly involves the differentiation of type 2 T helper (Th2) cells and the production of distinct type 2 cytokines, including interleukin-4 (IL-4), IL-5, and IL-13. Group 2 innate lymphoid cells (ILC2s) were recently recognized as another important source of type 2 cytokines. Although eosinophils, mast cells, and basophils can also express type 2 cytokines and participate in type 2 immune responses to various degrees, the production of type 2 cytokines by the lymphoid lineages, Th2 cells, and ILC2s in particular is the central event during the type 2 immune response. In this review, we discuss recent advances in our understanding of how ILC2s and Th2 cells orchestrate type 2 immune responses through direct and indirect interactions. Keywords: Type 2 immune response; type 2 T helper cell (Th2); Group 2 innate lymphoid cell (ILC2); Allergy and asthma Cellular & Molecular Immunology (2019) 16:225-235; https://doi.

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Section: Type 2 Immune Response Mediated By Ilc2smentioning

confidence: 99%

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

2019

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Section: Study Participants and Samplingmentioning

confidence: 99%

Innate lymphoid cell composition associates with COVID-19 disease severity

García

Kokkinou

García

et al. 2020

Preprint

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Objectives: The role of innate lymphoid cells (ILCs) in coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is unknown. Understanding the immune response in COVID-19 could contribute to unravel the pathogenesis and identification of treatment targets. To describe the phenotypic landscape of circulating ILCs in COVID-19 patients and to identify ILC phenotypes correlated to serum biomarkers, clinical markers, and laboratory parameters relevant in COVID-19. Methods: Blood samples collected from moderately (n=11) and severely ill (n=12) COVID-19 patients as well as healthy control donors (n=16), were analyzed with 18-parameter flow cytometry. Using supervised and unsupervised approaches, we examined the ILC activation status and homing profile. Clinical and laboratory parameters were obtained from all COVID-19 patients and serum biomarkers were analyzed with multiplex immunoassays. Results: ILCs were largely depleted from the circulation of COVID-19 patients compared with healthy controls. Remaining circulating ILCs from patients revealed increased frequencies of ILC2 in moderate COVID-19, with a concomitant decrease of ILC precursors (ILCp), as compared with controls. ILC2 and ILCp showed an activated phenotype with increased CD69 expression, whereas expression levels of the chemokine receptors CXCR3 and CCR4 were significantly altered in ILC2 and ILCp, and ILC1, respectively. The activated ILC profile of COVID-19 patients was associated with soluble inflammatory markers, while frequencies of ILC subsets were correlated with laboratory parameters that reflect the disease severity. Conclusion: This study provides insights into the potential role of ILCs in immune responses against SARS-CoV-2, particularly linked to the severity of COVID-19.

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“…We showed that among hepatic leukocytes, ILC2 constituted a very small population in liver homeostasis that was characterized by low expression of KLRG1, CD25, and GATA3 thereby resembling naive ILC2 29 . Elevated IL-33 levels have been shown in patients with acute and chronic liver inflammation [15][16][17][18][19] , suggesting that this cytokine plays a role in liver disease pathology.…”

Section: Discussionmentioning

confidence: 93%

Hepatic ILC2 activity is regulated by liver inflammation-induced cytokines and effector CD4+ T cells

Steinmann

Schoedsack

Heinrich

et al. 2020

Sci Rep

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In the present study, we investigated the phenotype and plasticity of hepatic ILC2 in response to liver inflammation-induced cytokines and effector CD4 + T cells in order to identify mechanisms of ILC2 regulation in liver disease. Material and Methods Mice. C57BL/6 mice and OT-II mice were bred in the University Medical Center Hamburg-Eppendorf animal facility (Hamburg, Germany). Mouse experiments were conducted according to the German animal protection law and approved by the institutional review board (Behörde für Gesundheit und Verbraucherschutz, Hamburg, Germany; G44/15). Mice received humane care according to the national guidelines of the National Institutes of Health in Germany. Animal treatment. C57BL/6 mice received intraperitoneally recombinant murine (rm)IL-33 (0.3 μg; BioLegend, San Diego, CA) daily on four consecutive days. ConA (7 mg/kg; Sigma-Aldrich, St. Louis, MO) was injected intravenously into C57BL/6 mice that were analyzed 8 and 24 hours later. Heart blood was drawn from individual mice and liver injury was quantified by automated measurement of plasma activities of alanine transaminase (ALT) using a COBAS Mira System (Roche Diagnostic, Mannheim, Germany). Immunohistochemistry. Liver samples were fixed with 4% formalin and embedded in paraffin. 3 μm liver sections were cut, stained with H&E following standard protocols, and analyzed by light microscopy. Isolation of hepatic ILC2 and CD4 + T cells. Hepatic non-parenchymal cells were isolated from livers of naive and IL-33-treated mice by Percoll density gradient centrifugation. Single cell suspensions were stained with the Lineage Antibody Cocktail (APC; BD Pharmingen, Heidelberg, Germany) as well as anti-Sca-1 (Pacific Blue; D7; BioLegend) and anti-ST2 (PerCP-eFluor 710; RMST2-2; ThermoFisher Scientific, Waltham, MA) antibodies. Lineage-negative (lin −) cells were enriched by magnetic cell sorting and lin − Sca-1 + ST2 + ILC2 were purely isolated by FACS (BD FACSAriaTM III sorter, BD Biosciences). Ovalbumin (OVA)-specific CD4 + T cells were isolated from spleen and lymph nodes of OT-II mice. Therefore, CD4 + T cells were enriched from single cell suspensions using the CD4 + T Cell Isolation Kit (Miltenyi Biotec, Bergisch Gladbach, Germany). Subsequently, cells were stained with anti-TCRβ (PE-Cy7; H57-597) and anti-CD4 (BV421; GK1.5; both BioLegend) antibodies and TCRβ + CD4 + T cells were purified by FACS.

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T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice

Cited by 42 publications

References 64 publications

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

Orchestration between ILC2s and Th2 cells in shaping type 2 immune responses

Innate lymphoid cell composition associates with COVID-19 disease severity

Hepatic ILC2 activity is regulated by liver inflammation-induced cytokines and effector CD4+ T cells

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